Hypertrophy of existing myocytes occurs with cardiac enlargement in the adult mammal. Although a variety of structural changes have been found with cardiac hypertrophy, changes in myocyte geometry have been difficult to determine in whole sectioned tissue. The specific aim of this project is to determine if changes in myocyte geometry reflect the type of cardiac workload. The hypothesis is that cell length is primarily affected with volume overload whereas changes in cell diameter are more evident in pressure overload. Isolated myocytes will be used to compare differences in cell length, width and volume from hyperthyroid, propranolol treated hyperthyroid, control, propranolol treated, and hypertensive (DOCA-salt) rat hearts. A sonic digitizer will be used to trace boundaries of isolated myocytes to determine cellular dimensions. Hyperthyroidism produces an increased cardiac output due primarily to tachycardia. Normalization of heart rate in hyperthyroid rats with propranol should produce a model of increased stroke volume for comparison with the hyperthyroid and hypertensive groups. Additionally, the cellular changes after reversal of hypertension and hyperthyroidism will be evaluated to determine if myocytes are reduced to a normal size or if they remain enlarged (normal heart size with larger myocytes would indicate cell death). Hearts from each group will also be perfusion fixed for morphometric evaluation of mitochondrial/myofibril ratio. In addition, hydroxyproline concentration will be measured in each group to determine the effects of this protocol on connective tissue content. The results of this study should provide important new information regarding the effect of different types of workload on the structural reorganization of the heart.